Bullock A N, Fersht A R
Department of Biochemistry, University of Washington, Seattle, USA.
Nat Rev Cancer. 2001 Oct;1(1):68-76. doi: 10.1038/35094077.
One protein--p53--plays nemesis to most cancers by condemning damaged cells to death or quarantining them for repair. But the activity of p53 relies on its intact native conformation, which can be lost following mutation of a single nucleotide. With thousands of such mutations identified in patients, how can a future cancer drug buttress this fragile protein structure and restore the cell's natural defence?
一种名为p53的蛋白质对大多数癌症起到克星的作用，它会判定受损细胞死亡或将它们隔离以便修复。但是p53的活性依赖于其完整的天然构象，而单个核苷酸的突变就可能导致这种构象丧失。在患者中已发现数千种此类突变，未来的抗癌药物如何才能支撑这种脆弱的蛋白质结构并恢复细胞的天然防御呢？
